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Chinese Journal of Kidney Disease Investigation(Electronic Edition) ›› 2013, Vol. 02 ›› Issue (06): 310-314. doi: 10.3877/cma.j.issn.2095-3216.2013.06.007

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New mechanism of renal tubulointerstitial fibrosis in sight of glycosylation

Hong-li LIN1,(), Da-peng WANG1   

  1. 1.Department of Nephrology,First Affiliated Hospital of Dalian Medical University,Dalian 116011,China
  • Online:2013-12-15 Published:2024-11-27
  • Contact: Hong-li LIN

Abstract:

Activation of transforming growth factor-β (TGF-β) signaling and proteinuria are two important pathways leading to renal tubulointerstitial fibrosis, Lin et.al from Dalian Medical University found that glycosylation may play a key role in renal tubulointerstitial fibrosis caused by activiatiion of TGF-β signaling or proteinuria. TGFβRII, a vital glycoprotein receptor in TGF-β signaling pathway, is modified by core fucosylation. Blocking the core fucosylation of TGFβRII could significantly inhibit activation of TGF-β signaling pathway, thereby inhibiting both the epithelial mesenchymal transition(EMT) of human kidney-2(HK-2) renal tubular epithelial cells and renal tubulointerstitial fibrosis of unilateral ureteral obstruction(UUO) rats caused by TGF-β1. Megalin receptor, which promotes renal fibrosis through excessive absorption of albumin in proteinuria, can also be modified by core fucosylation. Inhibition of the core fucosylation of megalin could block HK-2 cells apoptosis and inflammation caused by albumin overload,while high expression of core fucosylated megalin promoted cell apoptosis and inflammation. The above studies have for the first time explained the mechanism of renal tubulointerstitial fibrosis progression in sight of glycobiology.

Key words: Glycosylation, Transforming growth factor-β, Renal tubulointerstitial fibrosis, Mechanism

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